Inhibitor of DNA Binding 1, Dominant Negative Helix-Loop-Helix Protein (ID1) Kits ELISA

Zebrafish Inhibitor of DNA Binding 1, Dominant Negative Helix-Loop-Helix Protein (ID1) interaction partners

1. Gain and loss of id1 function in vivo demonstrated that Id1 promotes stem cell quiescence. The increased id1 expression observed in neural stem cells in response to injury appeared independent of inflammatory signals.

Mouse (Murine) Inhibitor of DNA Binding 1, Dominant Negative Helix-Loop-Helix Protein (ID1) interaction partners

1. study shows a biomechanical role of Id1 in endothelial cells' uptake of lipid by down-regulating LDLR, which could help understand how oscillatory flow affects atherosclerotic development.

2. We show that expression of Id-1, a negative regulator of myogenesis, is enhanced in Dnmt1-deficient cultures, leading to enhanced transdifferentiation of myoblasts toward the osteogenic lineage. Thus, these studies demonstrate that Dnmt1 influences cellular identity and determines lineage fidelity.

3. a loss of CULLIN3 represents a common signaling node for controlling the activity of intracellular WNT and SHH signaling pathways mediated by ID1

4. These results reveal a E2F1/miR-17-92/ENH1/Id1 regulatory axis during myogenesis.

5. Id1 enables both Lewis lung carcinoma cells and the host microenvironment for an effective liver colonization.

6. adipose tissue-specific overexpression of Id1 causes age-associated and high-fat diet-induced obesity in mice. Id1 suppresses BAT thermogenesis by binding to and suppressing PGC1alpha transcriptional activity. Lack of Id1 increases beige gene and Ucp1 expression in the WAT in response to cold exposure. Furthermore, brown-like differentiation is increased in Id1-deficient mouse embryonic fibroblasts.

7. If Gfi1 levels fall below a threshold, Id1 expression increases and renders E2A unable to function, which prevents hematopoietic progenitors from engaging along the B lymphoid lineage

8. Id1 may promote cell cycle progression of endothelial progenitor cells (EPCs), and that Wnt2 may be important in Id1 regulation of the cell cycle of EPCs.

9. Differential role of Id1 in MLL-AF9-driven leukemia based on cell of origin

10. Collectively, our results suggest that ENH1 plays an important role in the activation of myogenesis through the repression of Id2 activity.

11. Data indicate that upregulation of E2-2 protein markedly attenuated the inhibitor of DNA-binding 1 (ID1)-mediated increase in endothelial progenitor cells (EPCs) proliferation and migration.

12. these findings demonstrate that loss of Id compensation leads to dysregulation of the hematopoietic transcriptional network and multiple defects in erythropoietic development in adult mice.

13. our results strongly suggest that Usp1 is involved in the regulation of centrosome duplication, at least in part via ID1, and Usp1 may exert its oncogenic activity, partially through inducing centrosome abnormality.

14. demonstrated that Id1 and E2-2 are critical regulators of EPCs function in vitro. Id1 interacts with E2-2 and relieves the E2-2-mediated repression of FGFR1 and VEGFR2 expression to modulate EPCs functions

15. Endothelial ID1 up-regulation in inflamed colonic mucosa is an adaptive response that modulates the severity of tissue injury.

16. these findings provide in vivo genetic evidence of Id1 functions as an oncogene in breast cancer

17. overexpression leads to systemic immunosuppression by downregulation of key molecules involved in dendritic cell differentiation and suppression of CD8 T-cell proliferation, thus promoting primary tumour growth and metastatic progression

18. ID1/3 are crucial regulators of the adaptive antioxidant-mitochondrial response that promotes beta cell survival during oxidative stress through a novel link to the NFE2L2-small MAF pathway.

19. Using genetically modified mice, we found that loss of Id1 inhibited t(8;21) leukemia initiation and progression in vivo by abrogating protein kinase B (AKT)1 activation, and that Id1 interacted with AKT1 through its C terminus.

20. We conclude that Id1 is potently angiogenic and can be up-regulated in endothelial progenitor cells

Human Inhibitor of DNA Binding 1, Dominant Negative Helix-Loop-Helix Protein (ID1) interaction partners

1. study shows a biomechanical role of Id1 in endothelial cells' uptake of lipid by down-regulating LDLR, which could help understand how oscillatory flow affects atherosclerotic development.

2. ID1 overexpression is associated with histological subtype, lymph node metastasis, and unfavorable cancerspecific survival in penile squamous cell carcinoma.

3. Low ID1 expression is associated with breast cancer.

4. ID1, CTCF and ELK1 may be associated with prostate cancer, and may be potential therapeutic targets for the treatment of this disease.

5. CaMKII can directly phosphorylate Beclin 1 at Ser90 to promote K63-linked ubiquitination of Beclin 1 and activation of autophagy; it also promotes K63-linked ubiquitination of inhibitor of differentiation 1/2 (Id-1/2) by catalyzing phosphorylation of Id proteins and recruiting TRAF-6

6. ID1 expression was associated with the proliferation, invasion and migration of SACC cells. The observed inhibition of SACC cell growth, invasion and migration following knockdown of ID1 expression in the present study, may have been due to restoration of the balance between oncogenic and tumor-suppressive effects resulting from changes in the expression of downstream genes or associated proteins.

7. The mutual correlation between the expression level of TWIST1 and ID1 might be a critical factor driving the process of the human odontoblasts' differentiation.

8. a loss of CULLIN3 represents a common signaling node for controlling the activity of intracellular WNT and SHH signaling pathways mediated by ID1

9. Id1 enables lung cancer liver colonization by activating an epithelial mesenchymal transformation program in tumor cells and establishing the pre-metastatic niche.

10. High ID1 expression is associated with breast cancer.

11. ID1 expression impacts the sensitivity of colon cancer cells to 5-FU and may be considered as a potential predictive marker in colorectal carcinoma treatment.

12. Reducing ID1 gene expression reduces metastatic spread of salivary gland neoplasms.

13. High ID-1 expression is associated with colorectal carcinoma.

14. ID1 expression was positively related to drug resistance of EGFR-TKI in non-small cell lung cancer.

15. MVD was determined by immunohistochemistry, and the expressions of mRNA and protein of inhibitor of differentiation-1 (ID1) and vascular endothelial growth factor (VEGF) were detected in gastric cancer.

16. ID1 down-regulation induced parallel changes in the IGF and AKT pathways. The crosstalk of these pathways may enhance malignant phenotypes in salivary gland cancer.

17. Results show that ID1, ID3 and IGJ genes are highly expressed in adult B-ALL and correlate with poor prognosis in Hispanic patients.

18. Our findings define an intricate E2F1-dependent mechanism by which Id1 increases thymidylate synthase and IGF2 expressions to promote cancer chemoresistance. The Id1-E2F1-IGF2 regulatory axis has important implications for cancer prognosis and treatment.

19. Peritoneal VEGF-A expression is regulated by TGF-beta1 through an ID1 pathway in women with endometriosis

20. Id-1, a protein repressed by miR-29b, facilitates TGFbeta1-induced EMT in human ovarian cancer cells and represents a promising therapeutic target for treating ovarian cancer.